This invention relates generally to the field of endovascular, thoracic and urological surgery, and relates to catheter balloon delivery stent procedures in particular. Over the last several decades, the treatment of vascular congestion and urological constrictions has been revolutionized by percutaneous balloon angioplasty methods and advances in catheter construction and treatment, which allow a surgeon to insert a simple catheter device along a blood vessel or urethra and surgically shave or mechanically expand the inner wall of the vessel or tubular organ where desired. Such procedures in most instances involve less risk than open surgery, and have proven effective in a wide range of circumstances. However, balloon angioplasty procedures involve some trauma to the vessel wall and this injury may trigger a complex sequence of cellular responses that in many cases lead to restenosis, or closing off, of the treated portion. Studies have reported incidences of restenosis as high as 35-50% following percutaneous transluminal angioplasty of coronary vessels, and incidence of 19-30% after treatment of peripheral lesions. It is therefore an active and major area of medical research to find methods and treatment devices which inhibit or prevent such restenosis.
Uncontrolled cellular proliferation and other factors such as migration of smooth muscle cells into surrounding tissue, and extracellular matrix production by proliferating cells have all been identified as factors which may contribute to the processes of restenosis. Thus, inhibiting any of these three factors may prove effective in preventing the restenosis or short term closing off of a dilated or recanaled vessel following balloon dilation.
The strategies for effecting such inhibition have evolved in three general classes. The first of these is to place a porous, radially expanding metal stent into the affected area to mechanically "hold open" the vessel or tubular organ. Another method involves placing an expandable barrier structure in combination with a stent within the vessel to seal off the inner surface tissue to minimize restenosis. The third strategy involves delivering treatment or medication locally to the affected regions of tissue in the vessel to inhibit stenotic growth processes.
Vascular stents of the first-mentioned class, such as those described and publicized by Palmaz offer good results in mechanically keeping a vessel open for a period of time. However, recent studies have shown that due to the large percentage of open surface or through-openings of these balloon-expanded or self-expanded stents, the same diseased cells which caused the stenotic lesion originally readily proliferate through the open stent structure, causing restenosis of the stented vessel. This process of restenosis has been reported to occur in three stages, or phases, as follows:
______________________________________ Phase I Replication of smooth muscle cells (SMCs) ______________________________________ 0-3 days within the medial layer of the vessel Phase II Migration of SMCs from the medial layer into 3-14 days the intimal surface Phase III Proliferation of SMCs within the neointima and from 7 days- adjoining non-affected areas of the vessel; these cells 1 month proliferate and grow back into the affected zone which has undergone dilation/stent placement ______________________________________
Various devices have been used or proposed, including porous balloons which are advanced along the vessel to the position of the region to be treated, or hydrogel-coated balloons. Delivery of material to the vessel wall has been enhanced by providing material sandwiched between an inner balloon and an outer porous balloon, so that inflation of the inner balloon ejects medication through the pores of the outer balloon against the vessel lining.
Among purely physical techniques for endoluminal treatment, there have long existed devices such as that shown in U.S. Pat. No. 4,562,596, wherein a thin lining is secured within the vessel to strengthen the wall and prevent aneurysm. Such lining may also act as a barrier against spread of tissue from the covered region of the wall, preventing migration along the vessel or into the bloodstream. Other techniques have been proposed, such as that of the published international application WO9404096 which involves unfurling a reinforced rolled sheet to radially expand it into a shape-retaining tube liner or stent, and that of U.S. Pat. No. 5,316,023 which involves expanding a web-like tubular structure within a vessel. The web-like structure is embedded in an expandable plastic material, which apparently relies on the embedded web for shape retention.
In addition to the foregoing approaches, localized drug delivery has been achieved by periadventitial deposition of an active agent to exploit local diffusion as the primary delivery mechanism. For example, heparin in a matrix material placed in the periadventitial space of arteries following injury has been shown to reduce neointima formation in the first week. Provision of materials in a silastic shell has also been found to be an effective mechanism of drug delivery.
While indwelling vascular liners may prove effective for control of tissue proliferation conditions and restenosis, the implementation of an endoprosthetic liner to be delivered percutaneously poses severe problems due to constraints of size necessary for inserting such a device, and of strength and uniformity necessary to undergo sufficient expansion from a small diameter. While the techniques of catheterization have been developed with much technological detail for the delivery of balloons, for taking of samples, and for the performance of mapping or ablation functions in cardiac tissue, the delivery and installation of a vascular liner would pose unique problems because its operation requires its final diameter to match that of the vessel. An angioplasty balloon is generally formed of highly non-elastic material which is inflated to a high positive pressure to a maximum, fixed, dilated outer diameter. Such balloons are inflated only temporarily to enlarge the stenotic area of the vessel. Pumping balloons for cardiac assistance need not exert such great forces and may be formed with much thinner walls, allowing them to be folded or wrapped to reduce their size and to achieve a small diameter for insertion.
A conventional vascular liner, on the other hand, has a resting state diameter equal to or about ten percent greater than the inner diameter of the vessel in which it is to reside. In order to advance a conventional vascular, graft intraluminally, particularly within small branching vessels to the site of application, it is necessary that it be rolled, folded, or otherwise made much smaller in order to pass through tortuous or disease-affected regions of the vessel.
Accordingly, it would be desirable to provide a vascular liner of enhanced utility to inhibit restenosis and having a small ratio of insertion diameter to expanded diameter.
It is also desirable to provide a vascular liner which is sufficiently compact for intraluminal insertion and installation, yet after insertion and installation maintains a uniform and functional cellular barrier membrane function with dimensional stability and strength.